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Three-dimensional MR tomography was used to examine the relationship between symptoms of trigeminal neuralgia and neurovascular compression of the nerve in 18 patients. The intensity of neurovascular interaction was classified according to neuroradiological criteria. We found that a radiologically defined compression or dislocation of the nerve by an artery was always associated with symptoms of trigeminal neuralgia. A simple contact between vessel and nerve, however, was also observed on the asymptomatic sides of 10 out of 18 patients. In 6 of 18 patients, in contrast, trigeminal neuralgia was present in spite of the absence of neurovascular contact. In accordance with a cited study based on autopsy and intraoperative findings, our findings indicate that, in a certain proportion of cases, trigeminal neuralgia may be caused by neurovascular compression alone, whereas in other cases, other pathogenetic factors may be involved to a varying degree or be even exclusively responsible for the development of trigeminal neuralgia. The possible significance of the method for a preoperative estimation of the success of microvascular decompression of the trigeminal nerve is discussed.

Prostaglandin E analogs have been shown to be effective in the treatment of refractory trigeminal neuralgia in patients with multiple sclerosis. Prostaglandin E inhibits the functions of T lymphocytes which are involved in the pathophysiology of cluster headache. Therefore, a double-blind, placebo-controlled, crossover study on the efficacy of misoprostol in chronic refractory cluster headache was performed. Eight patients were treated with 600 micrograms misoprostol and with placebo for a 2-week period. No differences in attack frequency, intensity, global impression, and side effects could be detected, suggesting that prostaglandin E analogs are not effective in the treatment of chronic cluster headache.

A therapeutic trial with polyvitamins and dichloroacetate (DCA) in combination with thiamine in a 13-year-old girl with complex I deficiency is reported. The polyvitamin therapy included thiamine, riboflavin, ascorbate, coenzyme Q 10 and carnitine. This therapeutic regine was used over a period of 17 months without any effect. Although DCA lowered the lactate concentration in blood and CNS--measured by magnetic resonance spectroscopy--no clinical benefit was achieved. After 20 weeks of DCA therapy a distal polyneuropathy with areflexia developed although 100 mg thiamine daily as comedication was given from the beginning of DCA therapy. Nerve conduction velocity of the peroneal nerve was not detectable, sensible evoked potentials of the tibialis posterious nerve were normal. This side-effect resolved completely within 6 months after omission of DCA. Our observation suggests a direct toxic effect of DCA only on the peripheral nervous system in our patient since several cerebral MRI and magnetic resonance spectroscopy studies showed no abnormalities. CONCLUSION. DCA lowers the lactate concentration in children with complex I deficiency of the respiratory chain in a dose of 100 mg/kg body weight without clinical benefit. Reversible peripheral polyneuropathy may develop under DCA therapy despite thiamine medication.

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